血清心肌肌球蛋白轻链Ⅰ测定在烧伤后心肌损伤诊断中的应用

采用30%Ⅲ度烧伤大鼠模型,动态检测了伤前及烧伤后血清心肌肌球蛋白轻链I(CMLC_1)含量及心肌酶谱(CK,AST 和 LDH)变化,以进行烧伤后心肌损伤的评价。结果表明 CMLC_1在烧伤后1小时即明显增高,以后持续增高,伤后12小时比对照值升高约20倍,至伤后24,48小时仍保持高水平,伤后72小时开始轻度下降。心肌酶谱则于伤后3小时开始显著升高,至伤后24,48小时已表现出明显下降的趋势,伤后72小时已接近对照水平。提示:CMLC_1迅速大幅度增高表明严重烧伤早期心肌即发生明显损伤,CMLC_1与心肌酶谱比较具有出现早、高敏感、高特异等特点,是评价烧伤后心肌损伤的一个可靠指标。     

血清心肌肌球蛋白轻链Ⅰ测定在烧伤后心肌损伤诊断中的应用

采用３０％Ⅲ度烧伤大鼠模型，动态检测了伤前及烧伤后血清心肌肌球蛋白轻链Ⅰ（ＣＭＬＣ１）含量及心肌酶谱（ＣＫ，ＡＳＴ和ＬＤＨ）变化，以进行烧伤后心肌损伤的评价。结果表明ＣＭＬＣ１在烧伤后１小时即明显增高，以后持续增高，伤后１２小时比对照值升高约２０倍，至伤后２４，４８小时仍保持高水平，伤后７２小时开始轻度下降。心肌酶谱则于伤后３小时开始显著升高，至伤后２４，４８小时已表现出明显下降的趋势，伤后７２小时已接近对照水平。提示：ＣＭＬＣ１迅速大幅度增高表明严重烧伤早期心肌即发生明显损伤，ＣＭＬＣ１与心肌酶谱比较具有出现早、高敏感、高特异等特点，是评价烧伤后心肌损伤的一个可靠指标。     

血清心肌肌球蛋白轻链I测定在烧伤后心肌损伤诊断中的应用

采用３０％Ⅲ度烧伤大鼠模型，动态检测了伤前及烧伤后血清心肌肌球蛋白轻链Ｉ（ＣＭＬＣ１）含量及心肌酶谱（ＣＫ，ＡＳＴ和ＬＤＨ）变化，以进行烧伤后民肌损伤的评价。结果表明ＣＭＬＣ１在烧伤后１小时即明显增高，伤后１２小时比对照升高约２０倍，至伤后２４，４８仍保持高水平，伤后７２小时开始轻度下降。心肌酸疼     

大剂量静脉补钙抢救氢氟酸烧伤合并氟中毒六例

氢氟酸 (ＨＦ)烧伤不仅局部 (皮肤及呼吸道 )损伤严重 ,还会因氟中毒及低钙血症而致死[1] 。大剂量补钙是救治ＨＦ烧伤的重要措施 ,现介绍如下。1.临床资料 :本组 6例ＨＦ烧伤患者 ,烧伤面积 0 .3%～8%ＴＢＳＡ ,其中Ⅲ度烧伤 5例 ,浅Ⅱ度烧伤 1例 ,均用清水冲洗 15ｍｉｎ左右后入院。早期切痂植皮及皮瓣转移 2例 ;早期切开引流 ,急性中毒期后切痂 2例 ;肉芽创面植皮 1例 ;浅Ⅱ度局部湿敷治疗 1例。2 .建立一条补钙专用的静脉通路 ,定时抽血 ,在严密监测血钙及临床症状的情况下大胆补钙。定时检查血清电解质、心肌酶谱变化 ,指导临床补钙。…     

家兔氢氟酸烧伤后血管活性物质含量的变化

不同浓度的氢氟酸可引起皮肤严重损害或造成全身中毒症状，甚至会因低血钙而危及生命。抢救氢氟酸烧伤氟中毒时全身应用钙剂治疗，钙剂对心肌损伤有一定的保护作用。有研究表明，血浆内皮素(ET)、血浆降钙素基因相关肽(cGRP)的含量与心血管功能有关，本观察了氢氟酸烧伤后钙剂治疗中血浆ET-1和cGRP在不同时段的动态变化及其特点，以期为临床治疗提供理论依据。     

牛磺酸对严重烧伤大鼠心肌损害的保护作用

目的　观察牛磺酸(Tau)对严重烧伤大鼠心肌损害的作用。　方法　将Wistar大鼠随机分为对照组(10只,不致伤)、烧伤组(60只)和Tau治疗组(60只)。后两组大鼠造成30%TBSAⅢ度烫伤(以下称烧伤),烧伤组伤后常规补液,Tau治疗组伤后腹腔注射Tau400mg/kg.于两组烧伤大鼠伤后1、3、6、12、24、48h检测其血浆中心肌肌钙蛋白T(cTnT)、丙二醛(MDA)的含量以及血浆、心肌组织中肿瘤坏死因子α(TNF- α)、血管紧张素Ⅱ(AngⅡ)的含量、心肌钙离子水平,用透射电镜观察心肌组织形态结构变化,并与对照组的上述指标进行比较。将烧伤组大鼠血浆TNF- α、AngⅡ检测结果分别与cTnT检测结果作相关性分析。　结果　烧伤组大鼠伤后3h起血浆cTnT水平较对照组(0.16±0. 03)μg/L显著升高(P<0. 01), 12h达峰值(6. 32±0. 41)μg/L, 48h仍显著高于对照组(P<0. 01).烧伤组伤后3—48h血浆MDA含量及心肌钙离子水平明显高于对照组(P<0. 01 );伤后6—48h血浆和心肌组织TNF- α含量显著高于对照组(P<0. 01);血浆及心肌组织中AngⅡ水平分别于伤后1—24h、3—24h明显高于对照组(P<0. 01).Tau治疗组上述指标在伤后多数时相点明显低于烧伤组(P<0. 01). 烧伤组大鼠伤后早期心肌肌丝断裂溶解、线粒体肿胀、嵴减少,Tau治疗组心肌组织接近正常。烧伤组     

多根肋骨骨折后的心肌酶谱改变分析

肋骨骨折(ribfracture)在胸部创伤中最为常见,两根以上肋骨骨折为多根肋骨骨折,心脏损伤在钝性胸部创伤中发生率为10%～16%,其中以心肌挫伤(myocardial contusion,MC)最为常见[1].心肌酶谱(myocardial enzymes,ME)改变可作为诊断MC的参考指标.笔者对65例肋骨骨折患者检测心肌酶谱含量的变化,以观察肋骨骨折与心肌挫伤的关系.     

氢氟酸烧伤患者的治疗

1991～ 2 0 0 0年 10年间我科共收治 2 1例氢氟酸烧伤患者 ,深感氢氟酸烧伤的治疗有其特殊性。典型病例 :患者男 ,2 0岁 ,浓度 5 5 %氢氟酸泄漏致双下肢、右眼灼伤 ,伤后 3ｈ入院。诊断 :(1)氢氟酸烧伤总面积 9% ,Ⅲ度 4 %ＴＢＳＡ ;(2 )右眼烧伤。急诊检测血钙 1.5 3ｍｍｏｌ/     

家兔氢氟酸烧伤后早期不同处理方式的比较

目的观察家兔氢氟酸烧伤后早期用不同方式处理的效果。方法33只家兔均用550g/L氢氟酸造成5%TBSA烧伤创面,随机分为3组。A组13只,静脉输注等渗盐水5ml·kg-1·h-1;B组10只,给予等渗盐水的同时在不同时相点静脉注射50g/L葡萄糖酸钙,每次20mg/kg;C组10只,处理方法同B组并于伤后0.5h手术切痂。各组兔均于伤前及伤后不同时相点抽静脉血检测血氟、血钙,统计其死亡率。结果(1)A、B组家兔伤后1.0h血氟浓度达峰值,分别为(8.37±262)、(8.59±2.25)mg/L,B组是伤前值的107倍。24.0h后B组低于A组(P<0.05)。C组伤后1.0h血氟浓度明显下降为(6.20±0.23)mg/L,与A、B组比较,差异有统计学意义(P<001)。(2)各组家兔血钙浓度伤后呈下降趋势,8.0或12.0h为低谷。与伤前值比较,12.0h时A组下降了46%,B组下降32%,C组下降26%,C组与A、B组比较,差异有统计学意义(P<0.01)。24.0h后各组血钙浓度开始回升。(3)A、B、C组家兔72h内死亡率分别为30.8%、12.5%、0.0%。结论家兔氢氟酸烧伤后早期采用补钙 切痂术,可以迅速降低体内血氟浓度,逆转氟中毒致死性低钙血症及多系统毒性损伤。     

复方红景天对大鼠高原严重烧伤后早期心肌损伤的保护作用

目的　观察高海拔 (3480m)地区大鼠 30 %TBSAⅢ度烧伤后心肌损害的程度 ,探讨使用复方红景天后对大鼠心肌损伤的作用机制。　方法　 10 4只Wistar大鼠 ,随机分为红景天组 (48只 )、盐水组 (48只 )、正常对照组 (8只 )。正常对照组大鼠不作烧伤和其他处理。红景天组伤前 1周向大鼠胃内灌注复方红景天液 4ml,2次 /d;盐水组同方法灌注等量等渗盐水。分别在伤后 3、6、12、2 4、4 8、72h(每时相点 8只大鼠 )剖腹抽血 ,检测大鼠心肌酶谱及动脉血气变化 ,再摘取大鼠心脏作病理学检查。　结果　烧伤后 3h盐水组大鼠心肌组织损害明显 ,随后逐渐减轻 ,伤后 72h接近正常对照组水平。红景天组与盐水组大鼠心肌酶谱值均明显高于正常对照组 (P <0.0 1),但红景天组则明显低于盐水组 (P <0.0 1)。血气分析 :pH值 :盐水组与红景天组均低于正常对照组 (P <0.0 5 ),红景天组伤后 12～ 2 4h高于盐水组 (P <0.0 5)。剩余碱 :盐水组与红景天组均明显低于正常对照组 (P <0.0 1)。红景天组伤后 6h后高于盐水组 (P <0.0 5～ 0.0 1)。二氧化碳分压 :盐水组与红景天组均明显低于正常对照组 (P <0.0 5～ 0.0 1),伤后 4 8h红景天组 (35 .70± 4 .2 3)mmHg(1mmHg =0.133kPa)与正常对照组 (37.5 0± 6 .5 3)mmHg比较 ,差异无显著性意义     

液体复苏加山莨菪碱对烧伤兔心肌功能的影响

目的 探讨山莨菪碱对烧伤兔心肌功能的影响。方法 采用新西兰兔２５％Ⅲ度烫伤模型，分别于伤前，伤后即刻１，３，５，７小时测定左心室内压峰值，左心室内压最大变化速率，并观察严重烧伤休克期液体复苏加山莨菪碱对上述指标的影响。结果 严重烧伤后早期即发生心肌的收缩功能和舒张功能障碍，并呈进行性减退。单纯给予山莨菪碱或单纯输液治疗对兔严重烧伤后的心功能在短期内有支持作用，但治疗效果欠佳，且单纯山莨菪碱治疗组心     

烧伤血清对大鼠心肌细胞钙稳态的影响

目的　观察烫伤血清对成年大鼠分离的心肌细胞游离钙浓度 [(Ca2 )i]及胞膜钙通道电流的影响 ,探讨烧伤引起的心肌细胞钙稳态变化。　方法　伤后 2、4、6h分离 30 %TBSAⅢ度烧伤SD大鼠血清 ,简称 2hBS、4hBS、6hBS ;逆行循环灌流、胶原酶消化分离心肌细胞 ;Fura - 2 /AM荧光染色法测定 [Ca2 ]i;膜片钳技术全细胞记录模式测定细胞膜钙通道电流。　结果　正常心肌细胞[Ca2 ]i为 (10 1.3± 2 1.3)nmol/L ,烧伤血清可使心肌细胞 [Ca2 ]i显著升高。 (P <0 .0 1) ,以 6hBS的作用最强 ;钙通道阻断剂异搏定 (30mmol/L)和肌浆网rynodine受体拮抗剂普鲁卡因 (2mmol/L)均非常显著地抑制 6hBS的作用 (P <0 .0 1) ,抑制率分别为 47.7%和 6 7.6 % ,后者强于前者 (P <0 .0 1) ,2hBS使峰值L型钙电流 (ICa -L)比对照组增加 5 0 80 % ;而 6hBS使峰值ICa -L增加 1 5 2 .5倍 ;峰值电流 -电压曲线显示烧伤血清明显增加各个去极化钳制电压下的ICa ,并使得最大激活电压提前 ;细胞外液灌洗可祛除烧伤血清对钙电流的作用。　结论　烧伤血清能使心肌细胞 [Ca2 ]i,和膜上钙通道电流显著升高 ,钙稳态变化可能是烧伤后心肌损害的一种细胞机制     

钙分布异常对烧伤早期心肌力学障碍的影响

OBJECTIVE: To investigate the effect of abnormal Ca2+ distribution on impairment of myocardial mechanics in the early stage of thermal injury. METHODS: Calcium (Ca2+) changes were observed within subcellular distribution in situ in rat heart with calcium cytochemical probe and electron probe microanalysic technique. Meanwhile, myocardial mechanics and energy metabolic changes were investigated after thermal injury. RESULTS: The results demonstrated that levels of cytoplasmic Ca2+ in cardiomyocytes increased at 1 hour, followed by enhanced mitochondrial Ca2+ at 3 hour after burn injury. Parallel to the changes in Ca2+, there were decrease of myocardial contraction, relaxation capacity and increase of ventricular wall stiffness in burned rats. A lower level of heart energy changes was observed from 6 to 12 hours, compared with control group. CONCLUSION: The results indicate that subcellular Ca2+ abnormal distribution in myocardium caused by burn injury may be associated with rigor contraction and decreased relaxation of myocardium.     

Ruthenium red attenuated cardiomyocyte and mitochondrial damage during the early stage after severe burn

OBJECTIVE: To investigate the effects of ruthenium red on cardiomyocyte and mitochondrial damage during the early stage after severe burn. METHODS: Adult Wistar rats were randomized into normal control group (control), burn group (burns) and ruthenium red-treated group (RR) (n=8). Rats in the burn and RR groups were scalded to 30% TBSA III degree, and 30 min later, resuscitated with Ringer's solution. Ruthenium red was injected into rats of RR group at a dose of 2mg kg(-1), and again 3h later. Rats were sacrificed at the 6th hour post-scald, myocardial mitochondrial respiratory function and Ca(2+) concentration ([Ca(2+)](m)), serum creatine kinase (CK) and lactate dehydrogenase (LDH), myocardial ATP, ADP, AMP and lactate contents were determined. RESULTS: [Ca(2+)](m) in the RR group was significantly lower than that of the burn group. Mitochondrial respiratory control rate (RCR) and ST(3) were higher than those of burns, but ST(4) was high compared to the control group. Serum CK and LDH of the RR group decreased significantly, and were 65.0 and 45.5% of the burn group, myocardial ATP content in the ruthenium red-treated group increased by 100.4% and lactate level was decreased by 53.5% compared to the burn group. CONCLUSIONS: Ruthenium red attenuated myocyte and mitochondrial damage during the early stage after severe burns.     

磷烧伤后出血机理及钙剂治疗效果的实验研究

OBJECTIVE: To investigate the mechanism of hemorrhagic tendency after phosphorus poisoning. METHODS: 45% phosphoric acid and 20 mg/cm2 phosphorus were used to produce burn injury in rabbits. The total content of phosphorus remaining on the wound and 7-day mortality were similar in both groups. RESULTS: The results showed that plasma free calcium contents were significantly lower in both phosphorus groups than healthy and thermal burn controls (0.80 vs 1.40 mol/l, P < 0.01). The free calcium content of platelet was lowered to 116-140 nmol/l, which was significantly lower than that of healthy control (285 nmol/l) and thermal injury group (480-504 nmol/l). Concomitantly, the platelet aggregation rate was lowered to 1.29% and 10.78% in phosphoric acid group and phosphorus group, respectively, while it was 67.01% in healthy control and 82.1%-84.9% in thermal injury group; the difference was statistically significant. CONCLUSION: Calcium therapy brought back intracellular and extracellular free calcium contents to normal in phosphorus burn group. Also platelet aggregation rate approached normal level after calcium therapy. The results suggest that the bleeding tendency after phosphorus burn is due to combination of phosphorus with intracellular and extracellular calcium of platelets, thus inhibiting aggregation of platelets.     

Cardiac contraction and calcium transport function aftersevere burn injury in rats

Ａｄｅｃｒｅａｓｅｉｎｃａｒｄｉａｃｏｕｔｐｕｔｔａｋｅｓｐｌａｃｅｉｍｍｅｄｉａｔｅｌｙａｆｔｅｒｓｅｖｅｒｅｂｕｒｎｉｎｊｕｒｙ ,ａｎｄｉｆｔｈｅｄｅｃｒｅａｓｅｉｓｕｎｔｒｅａｔｅｄ ,ｌｏｗｃａｒｄｉａｃｏｕｔｐｕｔｃａｎｃｏｎｔｉｎｕｅｆｏｒｏｖｅｒ 2 4ｈａｎｄｉｎｄｕｃｅｓｏ ｃａｌｌｅｄｂｕｒｎｓｈｏｃｋｉｎｂｏｔｈｈｕｍａｎｂｅｇｉｎｓａｎｄａｎｉｍａｌｓ .Ｓｅｖｅｒａｌｓｔｕｄｉｅｓｈａｖｅｉｎｄｉｃａｔｅｄｔｈａｔｔｈｅｄｅｃｒｅａｓｅｄｃａｒｄｉａｃｃｏｎｔｒａｃｔｉｌｉｔｙ…     

The relationship between interferon-gamma and keratinocyte alloantigen expression after burn injury.

BACKGROUND: Cultured keratinocyte (CK) and cadaveric skin allografts have prolonged survival in patients with massive thermal injury. It is unclear if this delayed rejection is due to impaired host responsiveness or decreased graft immunogenicity. Although burn injury has been shown to decrease parameters of allograft response, no studies have examined the effect of burn injury on alloantigen expression. This study investigated the effect of burn size on class II antigen expression in CK allografts as well as on tissue levels of interferon-gamma (IFN-gamma), the principle regulator of alloantigen expression. METHODS: Anesthetized CBA mice (n = 64) received a 0%, 20% partial-thickness (PT), 20% full-thickness (FT), or 40% FT contact burn. Forty-eight hours later, wounds were partially excised and covered with CK allografts from C57BL/6 donors. Five days after burn injury, grafts were analyzed for donor-specific class II antigen. Protein expression was determined by Western immunoblotting and quantified with video densitometry. Wound, serum, and unburned skin levels of IFN-gamma were determined by enzyme-linked immunosorbent assay. Groups were compared by Fisher's analysis of variance. RESULTS: As burn size increased, class II antigen expression decreased (p < 0.001). This corresponded with decreased wound and skin levels of IFN-gamma after 40% burn (p < 0.05); however, wound IFN-gamma was significantly elevated after 20% PT and FT burns (p < 0.01). Serum IFN-gamma increased as burn size increased (p < 0.01). CONCLUSIONS: Burn injury decreases the antigenicity of CK allografts, which partly explains delayed allograft rejection after burn injury. Although wound IFN-gamma increases after minor thermal injury, the profound decrease in wound and skin IFN-gamma after a major burn corresponds with diminished class II antigen expression. The decreased availability of IFN-gamma after major thermal injury provides a mechanism for limited allograft tolerance.     

钙分布异常对烧伤早期心肌力学障碍的影响

目的探讨烧伤后早期心肌损伤的机理。方法应用Ｃａ２＋细胞化学探针及Ｘ线电子探针显微分析测定了烧伤后心肌细胞亚细胞Ｃａ２＋定位、定量变化，心肌力学及心肌组织能量代谢变化。结果烧伤后１小时心肌细胞胞浆Ｃａ２＋急剧升高，且先于线粒体Ｃａ２＋增加；伴心肌收缩、松弛能力下降，室壁应力增加。心肌组织ＡＴＰ、能量负荷在伤后６～１２小时显著低于对照组。结论烧伤后心肌细胞钙异常分布可能是引起心肌肌原纤维过强收缩，心肌松弛力降低的主要原因之一。